Natural Killer Cells in Viral Infection
In human and experimental animals, the outcome of a virus infection is determined by the infecting agent’s virulence and the host’s ability to limit virus spread. Both specific immune response and natural mechanisms of defense act in limiting infection. The efferent arm of the specific immune response may limit virus growth by various effector mechanisms: virus inactivation by antibodies, complement-mediated lysis of enveloped viral particles or virus-infected cells coated with appropriate antibody, lysis of infected cells by antibody-dependent cytotoxic cells or specific cytotoxic T lymphocytes (CTL). T cells have virtually no detectable spontaneous cytotoxic activity. Generation of CTL requires activation of T cells by antigen presented on accessory cells such as macrophages. Usually, a lag period of 7 to 10 days is required before T cells develop peak primary reactivity, which rapidly abates. An accelerated memory response of T cells occurs in 2 to 5 days upon reexposure to the antigen. Antibody-dependent cell-mediated cytotoxicity (ADCC) can be mediated by different kinds of leukocytes bearing receptors of the Fc portion of IgG molecules, including monocytes, polymorphonuclear leukocytes (PMN), and a subset of lymphocytes, without the requirement of prior activation. ADCC, however, as well as complementmediated lysis of infected cells, requires the presence of antibodies specific for structures expressed at the surface of the infected cells.
KeywordsToxicity Hepatitis Leukemia Influenza Sarcoma
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